Kivonat:
Insulin sensitivity and metabolic homeostasis depend on the capacity of adipose tissue to take up and utilise excess glucose and fatty acids. The key aspects that determine the fuel-buffering capacity of adipose tissue depend on the physiological levels of the small redox molecule, nitric oxide (NO). In addition to impairment of NO synthesis, excessive formation of superoxide (capital O, Cyrillic2 *- ) in adipose tissue may be an important interfering factor diverting the signalling of NO and other reactive oxygen and nitrogen species (ROS/RNS) in obesity, resulting in metabolic dysfunction of adipose tissue over time. Besides its role in relief from superoxide burst, enhanced NO signalling may be responsible for the therapeutic benefits of different superoxide dismutase mimics in obesity and experimental diabetes models. This review summarises the role of NO in adipose tissue and highlights the impact of NO/capital O, Cyrillic2 *- ratio "teetering" as a promising pharmacological target in metabolic syndrome. This article is protected by copyright. All rights reserved.
